Dentists and other professionals involved with the science of oral hygiene have dealt with a number of symptoms or pathologies of the mouth, gum and teeth. Some of these pathologies are initiated and exacerbated through tobacco consumption, whether smoked or chewed, as smokers often suffer from leukoplakia, a white patch on the buccal mucosa. Although leukoplakia is a benign oral lesion, it has a malignant potential requiring a biopsy of the lesion to rule out cancer. Smokers also have more dental tartar (calculus) than non-smokers and often suffer from halitosis.
It is known that tooth loss can directly result from untreated destructive periodontal (gum) disease. Further, acute necrotizing ulcerative gingivitis is a destructive, painful inflammatory condition which is, again, more acutely observed in cigarette smokers and tobacco users.
Besides leukoplakia, another type of generalized whitish hue on the buccal mucosa is associated with oral submucous fibrosis. This disease occurs mainly in India and Pakistan and their emigres to the western world and is a chronic, progressive, pre-malignant condition, related to tobacco and betel nut chewing.
Periodontal disease, which includes inflammation of the gums, is one of the most prevalent health problems in the world and is the major cause of tooth loss in the adult population.
Periodontal disease is composed of two entities:
a) Gingivitis: Inflammation is confined to the gums (gingival tissue). PA1 b) Periodontitis: The inflammation and infection is present both in the gingiva and in the connective tissue which supports the teeth.
There is initially an inflammation in the local blood vessel walls (vasculitis) which accounts for the most common symptom of bleeding gums. This is accompanied by migration of white blood cells (leucocytes) to help combat the tissue invasion by pathogenic mouth bacteria. In this inflammatory reaction, most cells liberate histamine. Inflammatory (white blood cells) also locally generate countless free radicals and anti-enzyme molecules, both of which contribute to tissue pathology. Collagen production may also then be interfered with due to local Vitamin C deficiency, which contributes to the swelling (edema) and redness (erythema) of gingival tissues.
Chewing tobacco and the areca nut are associated with higher frequencies of periodontal disease, oral submucous fibrosis and oral malignancies. Betel Quid chewing is common in India, Southeast Asia and the South Pacific Islands. Free radical damage induced by these deleterious alkaloids initiate an inflammatory reaction in the oral cavity. Studies in Taiwan reveal that arecoline, the major alkaloid in areca nut interferes with the migration, attachment and growth of human gingival fibroblasts. Arecoline also inhibits these cells' ability to synthesize collagen and all these inhibitory effects have been shown to be associated with an intracellular depletion of L-glutathione (GSH). The repeated and long term exposure to Betel Quid's cytotoxic arecoline and tobacco chewing renders these abusers to periodontal and other oral disease, in part due to losses of the locally vital protective antioxidant and detoxificant, GSH.
Prencipe et al. disclose an anti-bacterial, anti-plaque dentifrice in their U.S. Pat. No. 5,424,059. The '059 patent teaches that plaque can be inhibited and that gingivitis and cavities can be reduced or inhibited by applying a dentifrice in the form of a white water soluble alkaline earth metal polishing agent such as dicalcium phosphate or dimagnesium pyrophosphate used together with an anti-bacterial agent and the polyol, xylitol.
Galiana Arano in WO96/38122 discloses a novel dentifrice composition in the form of a tablet for buccal hygiene which does not require a toothbrush, toothpaste or dental powder. The tablet comprises an abrasive and foaming agent, sugar, one or more lubricants, a fluoride source and sweeteners. It is taught that the cleansing effect of water is obtained from the saliva stimulated by sugars while the mechanical effect of "brushing" is obtained from the granules emanating from the destruction of the tablet.
However, prior attempts to treat gum disease have failed for they have not recognized the role played by free radicals. For example, cigarette tar contains high concentrations of free radicals. The most common oxidants include semiquinone which is in equilibrium with hydroquinones and quinones, particularly in the viscous tar matrix. Many tar extracts are water soluble and reduce oxygen to the superoxide radical which can dismutate to form H.sub.2 O.sub.2. Importantly, glass-fiber type cigarette filters retain almost all of the tar particles that are larger than 0.1 micron. Thus, the filter acts as a trap for tars and cigarette smoke. There are an inordinately large number of free radicals, greater than 10.sup.15, in each puff of the gas phase of cigarette smoke. While the oxidants in tar are stable, those organic radicals in the gas phase smoke are reactive carbon and oxygen centered radicals with extremely short half-lives. Interestingly, concentrations of free radicals are maintained at high levels for more than ten minutes and tend to increase as tobacco smoke is aged. It is thus considered that these gas phase smoke oxidants are in a steady state as they are both continuously formed and destroyed. The latter reactions are similar to those noted to occur in smog, pointing to the extra noxious stimuli to primary and secondary smokers in polluted environments. In fact, environmental pollution in urban areas such as London, New York, Los Angeles and Mexico City promote gum disease and enhance the damage done to the oral cavity through the consumption of tobacco products. There is now also an established association between gum disease and coronary artery (heart) disease.
It is thus an object of the present invention to provide a gel, paste, gum or lozenge intended to be applied to the gums and teeth of a patient or taken orally as a means of preventing and ameliorating signs and symptoms and complications to the oral-pharyngeal cavity and mouth including the buccal mucosa and gums from damage caused by free radical species generating inflammation in gingival tissues.
These and further objects will be more readily apparent when considering the following disclosure and appended claims.